Abstract

The toxic effects of ammonia upon cellular metabolism have been demonstrated in many in vitro preparations (1-4). Further, elevated arterial levels of ammonia have been associated with the various manifestations of hepatic coma (5, 6). When ingestion of nitrogenous precursors was shown to elevate blood concentrations of ammonia in cirrhotic patients, the gastrointestinal tract was implicated as a source for circulating ammonia, at least in those with hepatic dysfunction (7, 8). Much of this formation of ammonia in the gut has been attributed to the breakdown of urea by bacterial ureases (9).